Effect of Tongxinluo on the expression of endogenous nestin and basic fibroblast growth factor after cerebral ischemia-reperfusion injury in rats

Objective To investigate the effect of Tongxinluo on the expression of endogenous nestin and basic fibroblast growth factor(bFGF) after cerebral ischemia-reperfusion injury in rats.Methods Ischemia was induced by temporary middle cerebral artery occlusion(MCAO),which was divided into model group,high dose group of Tongxinluo(1g·kg~(-1)·d~(-1)),low dose group of Tongxinluo(0.5 g·kg~(-1)·d~(-1)) and the sham operation group.The number of 5-Br deoxy uridine monophosphate (BrdU) and nestin in subventricle zone(SVZ) and dentate gyrus(DG) of rats at 3,5,7,14,21 and 30 days after MCAO were detected by immunohistochemistry and the bFGF mRNA were detected by RT-PCR at the same time.Results Almost there weren't BrdU+Nestin and bFGF mRNA expression in the sham operation group.Compared with model group,the immunofluorescin intensity of BrdU+Nestin increased at 5th day after MCAO in Tongxinluo high dose group and low dose group and achieved highest level at 14th day(P0.05).The bFGF mRNA expression in Tongxinluo high dose group and low dose group were significantly higher than that in model group at each time point(P0.05),and the higher level last to 30th day.The BrdU+Nestin in SVZ and DG of Tongxinluo high dose group was significantly higher than those in Tongxinluo low dose group at 5th,7th,14th,21 st and 30th day after MCAO(P0.05).The bFGF mRNA expression in Tonglxinluo high dose group and low dose group had significant diference compared with model group at the each time point(P0.05),but there was no statistic diference between Tongxinluo high dose group and low dose group(P0.05).Conclusions Cerebral ischemia-reperfusion injury can cause response and proliferation of neural stem cells in SVZ and DG of rats;Tongxinluo can enhance the ability of the differentiation and proliferation of neural stem cell in MCAO rats.Tongxinluo promote the expression of bFGF mRNA may be one of the mechanisms which promote the proliferation and differentiation of neural stem cells.